Effects of nicotine on distribution and release of 14C-norepinephrine and 14C-dopamine in rat brain striatum and hypothalamus slices

Goodman, Frank R.

doi:10.1016/0028-3908(74)90093-8

Cited by 74 publications

(12 citation statements)

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“…Most of them are heteroreceptors present, for example, on noradrenergic, dopaminergic and 5-hydroxytryptaminergic cell bodies and axons (Schwartz et al, 1984;Harfstrand et al, 1988). When stimulated, they increase the neuronal firing rate and transmitter release (Hall & Turner, 1972;Goodman, 1974;Giorguieff et al, 1979;Yoshida et al, 1980;Engberg & Swensson, 1980;Balfour, 1982;Westfall et al, 1983; 1 Author for correspondence. Egan & North, 1986;Rowell et al, 1987;Mereu et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

Nordberg

Romanelli

Sundwall³

et al. 1989

British J Pharmacology

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1 The effect of acute and chronic (16 days) administration of nicotine on cortical acetylcholine (ACh) release, gross behaviour and brain nicotinic binding sites was investigated in rats and guinea-pigs.2 The drug, injected either subcutaneously (0.45-0.90mgkg-1) or intracerebroventricularly (1, 3 and 5 ig) increased the cortical ACh release, in a dose-dependent manner, through mecamylaminesensitive receptors for 1-2 h in both species. 3 Chronic treatment significantly increased basal ACh release in the rat and slightly lowered it in the guinea-pig, but the response to a challenging dose of nicotine was proportionally maintained in both species. 4 The number of nicotinic receptors was four times higher in the rat than in the guinea-pig and was not dependent on the radioligand used ([3H]-nicotine or [3H]-ACh, in the presence of atropine) to determine this. The nicotinic binding sites showed an apparent increase in chronically treated rats but no change in guinea-pigs. 5 Tolerance to the inhibitory effect of the drug, assessed with the T maze test, was found in the rat. No apparent change in gross behaviour was detected in the guinea-pig. 6 It is concluded that chronic nicotine treatment causes evident tolerance to its inhibitory effect on behaviour in the rat, but no adaptation to its excitatory properties on the cholinergic brain structures in rats and guinea-pigs.

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Section: Introductionmentioning

confidence: 99%

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

Nordberg

Romanelli

Sundwall³

et al. 1989

British J Pharmacology

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“…Nicotine is also known to release a number of neurotransmitters (Balfour 1982). In the central nervous system, nicotinic receptor stimulation enhances release of norepinephrine from the hippocampus (Hall & Turner 1972;Goodman 1974) and dopamine from the limbic system (Imperato et a/. 1986) and striatal slices (Goodman 1974;Giorguieff et al 1979).…”

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confidence: 99%

“…In the central nervous system, nicotinic receptor stimulation enhances release of norepinephrine from the hippocampus (Hall & Turner 1972;Goodman 1974) and dopamine from the limbic system (Imperato et a/. 1986) and striatal slices (Goodman 1974;Giorguieff et al 1979). It also increases the release of acetylcholine from the cortex (Chiou et a/.…”

mentioning

confidence: 99%

Involvement of Cholinergic and Opioid Receptor Mechanisms in Nicotine‐Induced Antinociception

Zarrindast

Pazouki

Nassiri-Rad

1997

Pharmacology & Toxicology

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Abstract:In this work we have studied the influences of nicotinic agents on the antinociception of morphine in formalin test. Nicotine (0.001-0.1 mg/kg) induced antinociception in mice in a dose-dependent manner in the early phase of formalin test, and also potentiated the morphine effect. The nicotinic receptor antagonist, mecamylamine (0.5 mg/kg), but not hexamethonium decreased the antinociception induced by nicotine (0.1 mg/kg) in both phases. The muscarinic receptor antagonist atropine ( 5 and 10 mg/kg) also decreased the response of nicotine. Mecamylamine, hexamethonium or atropine did not alter morphine antinociceptive response, while naloxone decreased responses induced by nicotine or morphine. The antagonists by themselves did not elicit any response in formalin test, however, high doses of mecamylamine tend to increase pain response. It is concluded that central cholinergic and opioid receptor mechanisms may be involved in nicotine-induced antinociception.Nicotine has many effects on the central nervous system as alters spontaneous activity, brain excitability, heart rate and blood pressure and causes convulsions, antidiuresis and antinociception (Martin et al. 1983). Nicotine is also known to release a number of neurotransmitters (Balfour 1982). In the central nervous system, nicotinic receptor stimulation enhances release of norepinephrine from the hippocampus (Hall & Turner 1972;Goodman 1974) and dopamine from the limbic system (Imperato et a/. 1986) and striatal slices (Goodman 1974; Giorguieff et al. 1979). It also increases the release of acetylcholine from the cortex (Chiou et a/. 1970; Nordberg ef al. 1989). Muscarinic receptors have been suggested to be involved in analgesia (Chen 1958;Herz 1962;Harris et al. 1968). Nicotine-induced antinociception has been suggested to have different mechanisms than cholinergic-induced antinociception, even different mechanisms for the antinociceptive action of nicotine have been indicated (Tripathi et a/. 1982). There is also good evidence that nicotine is involved in activating opioid system(s) (Balfour 1982;Davenport et al. 1990 However, some investigators (Sahley & Berntson 1979) suggested that nicotine antinociception is mediated through the release of acetylcholine, others (Phan et a/. 1973) did not find evidence for antagonism by atropine in mice. The mechanisms of nicotine-induced antinociception are not fully understood. Our previous study showed that nicotine could attenuate naloxone-induced jumping in morphine-dependent mice (Zarrindast & Farzin 1996). In the present investigation, the possible role of cholinergic and opioid receptor mechanisms in nicotine-or morphine-induced antinociception have been studied. Materials and MethodsAnimals. Male Swiss albino mice weighing 20-25 g were used in groups of 10 in a light-controlled room (lights on 7 a m -7 p.m.) constant temperature (21 k2"C) . Animals had free access to food and water except during the experiments. Groups of 7-14 mice were used. The experimental protocol was approved by the Research a...

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“…It has been shown that baclofen depresses the firing rate of dopamine neurones in the substantia nigra and in the ventral tegmental area (Olpe et al 1977(Olpe et al & 1978 electrophysiological studies have established that nicotine causes an excitation of neurones in the ventral tegmental area (Grenhoff et al 1986;Mereu et al 1987). Nicotinic receptor stimulation enhances the release of dopamine from the limbic system (Imperato et al 1986) and striatal slices (Goodman 1974; Giorguieff et al 1979).Nicotinic (Martin et al 1983) and cholinergic (Iwamoto 1989; mechanisms have been suggested to be involved in the antinociception. However, whereas the role of monoamines in baclofen analgesia (Sawynok 1987) have been demonstrated, the role of nicotinic receptor mechanism(s) in baclofen antinociception has not been evaluated.…”

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confidence: 99%

“…Autoradiographic studies have shown that there are nicotinic binding sites on mesolimbic neurones (Clarke & Pert 1985) electrophysiological studies have established that nicotine causes an excitation of neurones in the ventral tegmental area (Grenhoff et al 1986;Mereu et al 1987). Nicotinic receptor stimulation enhances the release of dopamine from the limbic system (Imperato et al 1986) and striatal slices (Goodman 1974;Giorguieff et al 1979).…”

mentioning

confidence: 99%

Baclofen‐Induced Antinociception and Nicotinic Receptor Mechanism(s)

Sabetkasai

Ahang

Shafaghi

et al. 1999

Pharmacology & Toxicology

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Abstract:In this study, the influences of nicotinic receptor agents on baclofen-induced antinociception in the tail-flick test have been studied. Intraperitoneal administration of baclofen (2.5, 5 and 10 mg/kg) to mice induced a dose-dependent antinociception in the tail-flick test. Subcutaneous injection of nicotine (0.5-2.5 mg/kg) also caused a dose-dependent antinociceptive response. Intracerebral (10 and 20 pg/mouse) but not intraperitoneal administration of hexamethonium (5 and 10 mg/kg) to mice decreased the response of both nicotine and baclofen. However, administration of the GABAB antagonist CGP 35348 (100 and 200 mglkg) decreased the response induced by baclofen but not by nicotine. It is concluded that at least part of the baclofen-induced antinociception may be mediated through a nicotinic mechanism.It is well-established that y-amino butyric acid (GABA) is an important inhibitory synaptic transmitter in the vertebrate central nervous system. GABA receptors in the brain have been classified as GABAA and GABAB (Bowery et ul. 1980(Bowery et ul. & 1981Hill & Bowery 1981). Whereas GABAA receptors are directly associated with C1-channels, the GABAs receptors seem to be G-protein coupled and linked to Ca' ' or K' channels (Bormann 1988). A third class of GABA binding site, the GAB& sites, resembles the GA-BAA receptor but is insensitive to bicuculline (Drew et al. 1984: Johnston 1996.Baclofen is a derivative of GABA (DeFeudis 1977; Johnston 1978) and the prototype GABAB agonist (Bowery 1982). The drug has major clinical use as an antispastic agent (Young & Delwaide 1981), reduces pain associated with spasticity (Pinto et al. 1972), and is useful in the treatment of trigeminal neuralgia (Fromm et al. 1984).In rodent studies, baclofen can produce antinociception in a variety of tests (Sawynok 1987; Zarrindast & Moghadampour 1991;Sabetkasai et al. 1999), but the mechanism by which this occurs is only partially understood. It has been shown that baclofen depresses the firing rate of dopamine neurones in the substantia nigra and in the ventral tegmental area (Olpe et al. 1977(Olpe et al. & 1978 electrophysiological studies have established that nicotine causes an excitation of neurones in the ventral tegmental area (Grenhoff et al. 1986;Mereu et al. 1987). Nicotinic receptor stimulation enhances the release of dopamine from the limbic system (Imperato et al. 1986) and striatal slices (Goodman 1974; Giorguieff et al. 1979).Nicotinic (Martin et al. 1983) and cholinergic (Iwamoto 1989; mechanisms have been suggested to be involved in the antinociception. However, whereas the role of monoamines in baclofen analgesia (Sawynok 1987) have been demonstrated, the role of nicotinic receptor mechanism(s) in baclofen antinociception has not been evaluated.In the present work, the effects of the nicotinic agents on baclofen-induced antinociception in the tail-flick test has been examined. Materials and MethodsAnimals. Male albino mice (25-30 g) were used in the experiments. Animals were housed in plastic cages in an an...

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Effects of nicotine on distribution and release of 14C-norepinephrine and 14C-dopamine in rat brain striatum and hypothalamus slices

Cited by 74 publications

References 13 publications

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

Involvement of Cholinergic and Opioid Receptor Mechanisms in Nicotine‐Induced Antinociception

Baclofen‐Induced Antinociception and Nicotinic Receptor Mechanism(s)

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